Book contents
- Frontmatter
- Contents
- List of contributors
- List of abbreviations
- Preface to second edition
- 1 Definition, clinical features and neuroanatomical basis of dementia
- 2 Important anatomical landmarks in the brain in dementia
- 3 Practical approach to pathological diagnosis
- 4 Morphometric methods and dementia
- 5 Safety precautions in laboratories involved with dementia diagnosis and research
- 6 Molecular diagnosis of dementia
- 7 Neuropathology of the ageing brain
- 8 Neuroimaging Alzheimer's disease
- 9 Alzheimer's disease
- 10 Down's syndrome and Alzheimer's disease
- 11 Sporadic tauopathies: Pick's disease, corticobasal degeneration, progressive supranuclear palsy and argyrophilic grain disease
- 12 Hereditary tauopathies and idiopathic frontotemporal dementias
- 13 Vascular dementias
- 14 Familial and sporadic cerebral amyloid angiopathies associated with dementia and the BRI dementias
- 15 Parkinson's disease, dementia with Lewy bodies, multiple system atrophy and the spectrum of diseases with α-synuclein inclusions
- 16 Huntington's disease
- 17 Human prion diseases
- 18 Alcoholism and dementia
- 19 Hydrocephalus and dementia
- 20 Head injury and dementia
- 21 Infectious (and inflammatory) diseases causing dementia
- 22 Schizophrenia and its dementia
- 23 Other diseases that cause dementia
- 24 Transgenic mouse models of neurodegenerative disease
- Appendix: Dementia brain banks
- Index
21 - Infectious (and inflammatory) diseases causing dementia
Published online by Cambridge University Press: 12 October 2009
- Frontmatter
- Contents
- List of contributors
- List of abbreviations
- Preface to second edition
- 1 Definition, clinical features and neuroanatomical basis of dementia
- 2 Important anatomical landmarks in the brain in dementia
- 3 Practical approach to pathological diagnosis
- 4 Morphometric methods and dementia
- 5 Safety precautions in laboratories involved with dementia diagnosis and research
- 6 Molecular diagnosis of dementia
- 7 Neuropathology of the ageing brain
- 8 Neuroimaging Alzheimer's disease
- 9 Alzheimer's disease
- 10 Down's syndrome and Alzheimer's disease
- 11 Sporadic tauopathies: Pick's disease, corticobasal degeneration, progressive supranuclear palsy and argyrophilic grain disease
- 12 Hereditary tauopathies and idiopathic frontotemporal dementias
- 13 Vascular dementias
- 14 Familial and sporadic cerebral amyloid angiopathies associated with dementia and the BRI dementias
- 15 Parkinson's disease, dementia with Lewy bodies, multiple system atrophy and the spectrum of diseases with α-synuclein inclusions
- 16 Huntington's disease
- 17 Human prion diseases
- 18 Alcoholism and dementia
- 19 Hydrocephalus and dementia
- 20 Head injury and dementia
- 21 Infectious (and inflammatory) diseases causing dementia
- 22 Schizophrenia and its dementia
- 23 Other diseases that cause dementia
- 24 Transgenic mouse models of neurodegenerative disease
- Appendix: Dementia brain banks
- Index
Summary
Introduction
Dementia secondary to infectious disease, setting aside cases of transmissible spongiform encephalopathy (see Chapter 17) and the cognitive–motor abnormalities frequently associated with acquired immunodeficiency syndrome (AIDS), is distinctly unusual. Infectious disease as the primary cause of a dementing illness is usually a diagnosis of exclusion; lumbar puncture is often carried out in the clinical work-up of a demented patient – especially if the decline in mental status is rapidly progressive – in order to safely rule out a treatable infection (e.g. cryptococcal meningitis), unusual though this is, as the cause for a given individual's cognitive and neuropsychiatric decline. In a large experience of biopsies (approximately 5–10 per year) and autopsies (40–50 annually) carried out to establish the cause for dementia, we have rarely encountered – usually as a surprise finding – evidence of a central nervous system (CNS) inflammatory or infectious disease as the primary etiology. Such cases are, however, intriguing insofar as modern diagnostic tools can often establish an aetiological agent for the infection even when the only histopathological evidence for its existence (at autopsy) is widespread chronic inflammation of the brain and its overlying leptomeninges. Throughout the 1980s and 1990s, the range of known viruses and bacteria that target the CNS has widened substantially (Kennedy, 1990; Vinters et al., 1998). The availability of highly sensitive molecular diagnostic tests (especially the polymerase chain reaction, PCR), by which faint traces of molecular ‘footprints’ of bacterial or viral pathogens may be detected within neural tissue, allows the safe prediction that many new associations between micro-organisms and CNS/PNS disease will be made in the coming years (Darnell, 1993; Tompkins, 1992).
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- The Neuropathology of Dementia , pp. 472 - 496Publisher: Cambridge University PressPrint publication year: 2004